In order to understand the effects of developmental exposure to methyl/mercury on the ontogeny of synaptic function, the impact of prenatal or postnatal exposure on acquisition of receptor binding sites for norepinephrine was examined. The actions of the mercurial were both regionally - and receptor subtype-selective and depended upon the maturational profile of each region. Alpha 1 and alpha 2 and Beta-receptor sites in the cerebellum, the region which develops last, were the most vulnerable to methylmercury. In contrast, the same receptor subtypes in the midbrain + brainstem, which develops earliest, were resistant to methylmercury. The cerebal cortex, which matures at a time midway between cerebellum and midbrain + brainstem, also displayed intermediate vulnerability to actions of methylmercury on receptors. Within the cerebellum, prenatal exposure to 1 mg/kg to methylmercury, interfered the most with ontogeny of alpha 1-receptor binding, less so far alpha 2-receptors and least for Beta-receptors. Lower doses of methylmercury tended to increase receptor binding for all subtypes, a fact which may contribute to promotion of neurological development seen in animals exposed to those levels.